Mir-181b Functions as Anti-Apoptotic Gene in Post-Status Epilepticus via Modulation of Nrarp and Notch Signaling Pathway
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Updated: Mar 30, 2026

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
Published on: April 24, 2021
Chen Zhang1, Deren Hou2, Xialu Feng2
1Department of Neurology, Third Xiangya Hospital, Central South University, Changsha, China zhangchen1208@hotmail.com.
Background:
The expression pattern and function of miRs in the post-status epilepticus (SE) rat are still unclear. This study aimed to investigate the role and mechanism of miR-181b in the post- SE rat.
Methods:
The lithium-pilocarpine-induced SE model was established in Sprague-Dawley rats. The expression of miR-181b in rat blood and hippocampus was confirmed by RT-PCR at 24 hous and 7 days post-SE. The expression of Nrarp, Hes-1, and Bcl-2 was detected by RT-PCR and western blot. After the rat model was treated with LV-rno-mir181b and LV-anti-181b-5p, the expression change of miR-181b, Nrarp, Hes-1, and Bcl-2 was examined again. The effects of altering the expression of miR-181b on neurone cell apoptosis post-SE were assessed.
Results:
The expression of miR-181b significantly decreased both in post-SE rat hippocampus and peripheral blood at 24 hours and 7 days (p<0.05). Nrarp is up-regulated, however, Hes-1 and Bcl-2 are down-regulated (p<0.05). LV-miR-181b treatment induced down-regulation of Nrarp and up-regulation of Hes-1 and Bcl-2 (p<0.05). Neurone cell apoptosis decreased in miR-181b group and post-SE rat hippocampal (p<0.05).
Conclusions:
Our study showed the low-expression of miR-181b in the hippocampus in a post-SE rat model. MiR-181b negatively regulated Nrarp as an anti-apoptotic gene via Notch signaling pathway.
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